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Cited by 136Carcinogens and Genotoxicity AssessmentArsenic contamination and mitigationHeavy Metal Exposure and Toxicity

The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.

Arsenic induces oxidative DNA damage in mammalian cells

Kessel, Maris, Liu, Su Xian, Xu, An, Santella, Regina, Hei, Tom K.·2002·Molecular and Cellular Biochemistry
DOI 10.1023/a:1015927406142
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Abstract

Although arsenic is a well-established human carcinogen, the underlying carcinogenic mechanism(s) is not known. Using the human-hamster hybrid (A(L)) cell mutagenic assay that is sensitive in detecting mutagens that induce predominately multilocus deletions, we showed previously that arsenite is indeed a potent gene and chromosomal mutagen and that oxyradicals may be involved in the mutagenic process. In the present study, the effects of free radical scavenging enzymes on the cytotoxic and mutagenic potential of arsenic were examined using the AL cells. Concurrent treatment of cells with either superoxide dismutase or catalase reduced both the cytotoxicity and mutagenicity of arsenite by an average of 2-3 fold, respectively. Using immunoperoxidase staining with a monoclonal antibody specific for 8-hydroxy-2'-deoxyguanosine (8-OHdG), we demonstrated that arsenic induced oxidative DNA damage in A(L) cells. This induction was significantly reduced in the presence of the antioxidant enzymes. Furthermore, reducing the intracellular levels of non-protein sulfhydryls (mainly glutathione) using buthionine S-R-Sulfoximine increased the total mutant yield by more than 3-fold as well as the proportion of mutants with multilocus deletions. Taken together, our data provide clear evidence that reactive oxygen species play an important causal role in the genotoxicity of arsenic in mammalian cells.

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Research works printed but not linked: 11

  1. Axelson O: Arsenic compounds and cancer. In: V. Vainio (eds). Occupational Cancer and Carcinogenesis. Hemisphere Publishing Corporation, Washington, D.C., 1980, pp 1229–1235.
  2. U.S. EPA: Soil Screening Guidance Technical Background Document. Office of Solid Waste and Emergency Response. EPA/540/R-95/128. United States Environmental Protection Agency, Washington, D.C., 1996
  3. Dhar RK, Biswas BK, Samanta G: Groundwater arsenic calamity in Bangladesh. Curr Sci 73: 48–59, 1997
  4. Warner ML, Moore LE, Smith MT, Kalman DA, Fanning E, Smith AH: Increased micronuclei in exofoliated bladder cells of individuals who chronically ingested arsenic-contaminated water in Nevada. Cancer Epidem Biomarkers Prevent 3: 583–590, 1994
  5. IARC: Monograph on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Suppl. 4, 1982, pp 50–51
  6. Wang Z, Rossman TG: The carcinogenicity of arsenic. In: T. Chang (eds). Toxicology of Metals. CRC Press, Boca Raton, 1996, pp 221–229
  7. Hei TK, Piao CQ, He ZY, Vannais D, Waldren CA: Chrysotile fiber is a potent mutagen is mammalian cells. Cancer Res 52: 6305–6309, 1992
  8. Xu A, Wu LJ, Santella R, Hei, TK: Role of reactive oxygen species in the mutagenicity and DNA damage induced by crocidolite fibers in mammalian cells Cancer Res 59: 5615–5624, 1999
  9. Yarborough A, Zhang UJ, Hsu TM, Santella RM: Immunoperoxidase detection of 8-OHdG in aflatoxin B1-treated rat liver and human oral mucosal cells. Cancer Res 56: 683–688, 1996
  10. Applegate LA, Luscher P, Tyrrell RM: Induction of heme oxygenase: A general response of oxidant stress in cultured mammalian cells. Cancer Res 51: 974–978, 1991
  11. Engel RR, Hopenhayn-Rich C, Receveur O, Smith AH: Vascular effects of chronic arsenic exposure. Epidemiol Res 16: 184–208, 1994

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Metadata

Authors
Kessel, M., Liu, S. X., Xu, A., Santella, R., & Hei, T. K.
Affiliations
Columbia University (US)
Corresponding author
Hei, Tom K.
ORCID
Venue
Molecular and Cellular Biochemistry
Publisher
Springer Science and Business Media LLC
Published
2002-05
Volume
234-235
Issue
1
Pages
301-308
ISSN
  • 0300-8177 (ISSN-L)
  • 1573-4919
DOI
10.1023/a:1015927406142
OpenAlex
W4243944514
Cited by
135
References
30
Citations by year
2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 2 · 2021: 9 · 2020: 3 · 2019: 5 · 2018: 2 · 2017: 2 · 2016: 6 · 2015: 5 · 2014: 9 · 2013: 7 · 2012: 9
FWCI
3.39
Type
journal article
Language
en
Open access
closed
Licence
Locations
Molecular and Cellular Biochemistry (publishedVersion)
Funders
  • U.S. Environmental Protection Agency
  • National Institutes of Health
  • National Institute of Environmental Health Sciences (P42 ES10349, ES 08821, P30-ES09089)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
  • Physical Sciences › Environmental Science › Environmental Chemistry › Arsenic contamination and mitigation
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
Keywords
arsenic, arsenite, oxidative DNA damage, genotoxicity, carcinogenesis, reactive oxygen species, superoxide dismutase, catalase, antioxidant enzymes, 8-hydroxy-2'-deoxyguanosine, glutathione, buthionine sulfoximine, cytotoxicity, mutagenicity

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